Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA225587 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:miRNA array comparing the transcription profile of control rats and rats after intra-hippocampal pilocarpine-induced Status Epilepticus (PILO-SE).
2016-04-28 | E-MTAB-4633 | biostudies-arrayexpress
Project description:Temporal lobe epilepsy (TLE) can develop from alterations in hippocampal structure and circuit characteristics, and can be modeled in mice by administration of kainic acid (KA). Adult neurogenesis in the dentate gyrus (DG) contributes to hippocampal functions and has been reported to contribute to the development of TLE. Some of the phenotypical changes include neural stem and precursor cells (NPSC) apoptosis, shortly after their birth, before they produce hippocampal neurons. Here we explored these early phenotypical changes in the DG 3 days after systemic KA administration to mice. Our specific aim was to understand the molecular mechanisms underlying altered apoptosis levels in NSPC following KA-induced status epilepticus (KA-SE). Accordingly, we chose a multi-omics experimental setup and analyzed DG tissue samples using proteomics, transcriptomics and microRNA profiling techniques. We here present a description of how these date were obtained and provide them to others for further analysis and validation. This may help to further identify and characterize molecular mechanisms involved in the alterations induced shortly after KA-SE in the mouse DG. Total RNA obtained from dentate gyrus 72h after mice were subjected to repeated low dose kainic acid induced status epilepticus or saline i.p. injections
2016-03-12 | E-GEOD-79131 | biostudies-arrayexpress
Project description:Temporal lobe epilepsy (TLE) can develop from alterations in hippocampal structure and circuit characteristics, and can be modeled in mice by administration of kainic acid (KA). Adult neurogenesis in the dentate gyrus (DG) contributes to hippocampal functions and has been reported to contribute to the development of TLE. Some of the phenotypical changes include neural stem and precursor cells (NPSC) apoptosis, shortly after their birth, before they produce hippocampal neurons. Here we explored these early phenotypical changes in the DG 3 days after systemic KA administration to mice. Our specific aim was to understand the molecular mechanisms underlying altered apoptosis levels in NSPC following KA-induced status epilepticus (KA-SE). Accordingly, we chose a multi-omics experimental setup and analyzed DG tissue samples using proteomics, transcriptomics and microRNA profiling techniques. We here present a description of how these date were obtained and provide them to others for further analysis and validation. This may help to further identify and characterize molecular mechanisms involved in the alterations induced shortly after KA-SE in the mouse DG. Total RNA obtained from dentate gyrus 72h after mice were subjected to repeated low dose kainic acid induced status epilepticus or saline i.p. injections
2016-03-12 | E-GEOD-79129 | biostudies-arrayexpress
Project description:Transient brain insults including status epilepticus (SE) can initiate a process termed ‘epileptogenesis’ that results in chronic temporal lobe epilepsy (TLE). As a consequence, the entire tri-synaptic circuit of the hippocampus is fundamentally impaired. A key role in epileptogenesis has been attributed to the CA1 region as the last relay station in the hippocampal circuit and as site of aberrant plasticity, e.g. mediated by acquired channelopathies. The transcriptional profiles of the distinct hippocampal neurons are highly dynamic during epileptogenesis. Here, we aimed to elucidate the early SE-elicited mRNA signature changes and the respective upstream regulatory cascades in CA1. RNA sequencing of CA1 was performed in the mouse pilocarpine-induced SE model at multiple time points ranging from 6 to 72 hours after the initial insult. Bioinformatics was used to decipher altered gene expression, signalling cascades and their corresponding cell type profiles. Robust transcriptomic changes were detected at 6h after SE and at subsequent time points during early epileptogenesis. Major differentially expressed mRNAs encoded primarily immediate early and excitability-related gene products, as well as genes encoding immune signalling factors.
2023-12-20 | GSE241219 | GEO
Project description:microRNAs profiling in hippocampal cells of Self-Sustaining Status Epilepticus (SSSE) mouse model
| PRJNA225589 | ENA
Project description:The phosphorylation-based signalling and protein changes occurring in the early phases after a pathophysiological insult, like status epilepticus (SE), have not been detailed. In a companion project, the hippocampi of mice treated with pilocarpine and diazepam were examined by tandem mass tag (TMT11plex) mass spectrometry at 4 and 24 h post-status epilepticus (PXD038241). In the accompanying article, the results implicated posttranscriptional regulatory proteins as early targets of increased phosphorylation. Also, the major targets of decreased phosphorylation at 4 h and 24 h were a subset of post synaptic density scaffold proteins, ion channels and neurotransmitter receptors. Here, the earlier work is repeated on protein and phosphorylation site targets representative of the important SE-dependent changes using parallel reaction monitoring (PRM), supporting the main findings.
2024-02-22 | PXD047870 | Pride
Project description:Status Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures. Here we report an unbiased analysis of the hippocampal transcriptome of mice with targeted disruption of Dio2 in the astrocytes (Astro-D2KO mouse) undergoing 3 h SE.
2018-05-25 | GSE114887 | GEO
Project description:Purpose: to evaluate changes in the transcriptome of hippocampal cells during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Experimental Design: Gene expression profiling was analyzed in hippocampi of rats subjected to the pilocarpine model of epilepsy at different times during the course of epileptogenesis: 3 days post-SE (3D), 7 days post-SE (7D), and immediately (up to 12h) after the first spontaneous seizure (Chronic). All three pilocarpine subgroups had a corresponding age-matched control group (saline-treated rats), from which normal hippocampi samples were obtained at the same experimental time points. Independent microarray hybridizations were carried out for each sample (n = 5, per experimental group) with oligonucleotide microarrays covering 34,000 transcripts representing most of the known and predictive genes of the rat genome (CodeLink™ Rat Whole Genome Bioarrays, GE Healthcare), following the manufacturer’s protocol. Results: differential expression of almost 1,400 genes was detected during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Most of these genes are novel and displayed an up-regulation after SE. Noteworthy, a group of 128 genes functioning in neurogenesis, apoptosis, immune response, and intracellular signal transduction was found consistently hyper-expressed throughout epileptogenesis, indicating stable molecular alterations within the hippocampus. Those include modulation of the MAPK, Jak-STAT, PI3K, TGF-beta, and mTOR signaling pathways. Differential expression of genes from the p38 MAPK pathway, mediating inflammation and neurogenesis, was also confirmed by real-time PCR. These findings reveal dynamic molecular changes occurring in the hippocampus that may serve as a starting point for the generation of new hypothesis regarding the underlying mechanisms of epilepsy and for the designing of alternative therapeutic strategies. Keywords: gene expression changes during epileptogenesis.
2010-02-09 | GSE14763 | GEO
Project description:Purpose: to evaluate changes in the transcriptome of hippocampal cells during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Experimental Design: Gene expression profiling was analyzed in hippocampi of rats subjected to the pilocarpine model of epilepsy at different times during the course of epileptogenesis: 3 days post-SE (3D), 7 days post-SE (7D), and immediately (up to 12h) after the first spontaneous seizure (Chronic). All three pilocarpine subgroups had a corresponding age-matched control group (saline-treated rats), from which normal hippocampi samples were obtained at the same experimental time points. Independent microarray hybridizations were carried out for each sample (n = 5, per experimental group) with oligonucleotide microarrays covering 34,000 transcripts representing most of the known and predictive genes of the rat genome (CodeLink⢠Rat Whole Genome Bioarrays, GE Healthcare), following the manufacturerâs protocol. Results: differential expression of almost 1,400 genes was detected during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Most of these genes are novel and displayed an up-regulation after SE. Noteworthy, a group of 128 genes functioning in neurogenesis, apoptosis, immune response, and intracellular signal transduction was found consistently hyper-expressed throughout epileptogenesis, indicating stable molecular alterations within the hippocampus. Those include modulation of the MAPK, Jak-STAT, PI3K, TGF-beta, and mTOR signaling pathways. Differential expression of genes from the p38 MAPK pathway, mediating inflammation and neurogenesis, was also confirmed by real-time PCR. These findings reveal dynamic molecular changes occurring in the hippocampus that may serve as a starting point for the generation of new hypothesis regarding the underlying mechanisms of epilepsy and for the designing of alternative therapeutic strategies. Keywords: gene expression changes during epileptogenesis. We performed a genome wide analysis of genes differentially expressed during epileptogenesis. Virtually, all possible changes in the rat transcriptome were monitored at distinct time points corresponding to the latent to chronic phase transition of the pilocarpine model of epilepsy, which is probably the most extensively studied chemically inductive model of TLE. Genes identified as being differentially expressed were classified based on their respective biological functions to envisage processes and pathways likely implicated in epileptogenesis, as well as their possible value as targets for therapy. Results were expressed as fold variation, and genes displaying greater than 2-fold changes in transcript abundance and p<0.01 were selected.
2010-02-09 | E-GEOD-14763 | biostudies-arrayexpress
Project description:We performed gene expression profiling of FACS purified nuclei from hippocampal area CA1 from adult male mice (Calb1xTdtomato mice) subjected to kainic acid-induced status epilepticus (chronic epileptic phase) and control animals.
2021-05-28 | GSE143560 | GEO